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The design of future materials for biotechnological applications via deposition of molecules on surfaces will require not only exquisite control of the deposition procedure, but of equal importance will be our ability to predict the shapes and stability of individual molecules on various surfaces. Furthermore, one will need to be able to predict the structure patterns generated during the self-organization of whole layers of (bio)molecules on the surface. In this review, we present an overview over the current state of the art regarding the prediction and clarification of structures of biomolecules on surfaces using theoretical and computational methods.
Beta-ketothiolase deficiency, also known as mitochondrial acetoacetyl-CoA thiolase (T2) deficiency, is an autosomal recessive disease caused by mutations in the acetylCoA acetyltransferase 1 (ACAT1) gene. A German T2deficient patient that developed a severe ketoacidotic episode at the age of 11 months, was revealed to be a compound heterozygote of a previously reported null mutation, c.472A>G (p.N158D) and a novel mutation, c.949G>A (p.D317N), in ACAT1. The c.949G>A mutation was suspected to cause aberrant splicing as it is located within an exonic splicing enhancer sequence (c. 947CTGACGC) that is a potential binding site for serine/argininerich splicing factor 1. A mutation in this sequence, c.951C>T, results in exon 10 skipping. A minigene construct was synthesized that included exon 9truncated intron 9exon 10truncated intron 10exon 11, and the splicing of this minigene revealed that the c.949G>A mutant construct caused exon 10 skipping in a proportion of the transcripts. Furthermore, additional substitution of G for C at the first nucleotide of exon 10 (c.941G>C) abolished the effect of the c.949G>A mutation. Transient expression analysis of the c.949G>A mutant cDNA revealed no residual T2 activity in the mutated D317N enzyme. Therefore, c.949G>A (D317N) is a pathogenic missense mutation, and diminishes the effect of an exonic splicing enhancer and causes exon 10 skipping. The present study demonstrates that a missense mutation, or even a synonymous substitution, may disrupt enzyme function by interference with splicing.
Large bone defects require fabricated bone constructs that consist of three main components: an artificial extracellular matrix scaffold, stem cells with the potential to differentiate into osteoblasts, and bioactive substances, such as osteoinductive growth factors to direct the growth and differentiation of cells toward osteogenic lineage within the scaffold.
During the last 50 years, a broad range of visible light curing resin based composites (VLC RBC) was developed for restorative applications in dentistry. Correspondingly, the technologies of light curing units (LCU) have changed from UV to visible blue light, and there from quartz tungsten halogen over plasma arc to LED LCUs increasing their light intensity significantly. In this thesis, the influence of the curing conditions in terms of irradiance, exposure time and irradiance distribution of LCU on reaction kinetics as well as corresponding mechanical and viscoelastic properties were investigated.
Bisher ist nicht bekannt, in welchem Ausmaß Fremd- oder Störgerüche dazu geeignet sind, die allgemeine Leistungsfähigkeit eines Sprengstoffspürhundes einzuschränken oder sogar die Detektion eines Sprengkörpers zu verhindern. Ziel ist es zu untersuchen, inwieweit sich durch den gezielten Einsatz von Störsubstanzen die Sprengstoffdetektionsfähigkeit von Spürhunden beeinflussen lässt. Mit Detektionsfähigkeit ist hier sowohl die Wahrscheinlichkeit einer richtigen Detektion von Sprengstoffen in Gegenwart von starken Fremdgerüchen, als auch die ebenfalls zu erwartende Verringerung der Einsatzdauer (vorzeitige Erschöpfung) gemeint.
Brentuximab vedotin (SGN-35) is an antibody–drug conjugate with a high selectivity against CD30+ cell lines and more than 300-fold less activity against antigen-negative cells. In the last years, the results of many in vitro and in vivo studies have led to the fast approval of this drug to treat lymphoma patients. Another innovative method to treat tumor cells including lymphoma cells is the use cytokine-induced killer (CIK) cells, which have also been approved and proven to be a safe treatment with only minor adverse events. In this study, a possible additive effect when combining SGN-35 with CIK cells was investigated. The combinational treatment showed that it reduces the viability of CD30+ cell lines significantly in vitro. Additionally, the amount of lymphoma cells was significantly reduced when exposed to CIK cells as well as when exposed to SGN-35. A significant negative effect of SGN-35 on the function of CIK cells could be excluded. These results lead to the assumption that SGN-35 and CIK cells in combination might achieve better results in an in vitro setting compared to the single use of SGN-35 and CIK cells. Further investigations in in vivo models must be conducted to obtain a better understanding of the exact mechanisms of both treatments when applied in combination.